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Rewinding the clock with epigenomics

Researchers are uncovering epigenetic mechanisms that contribute to cellular reprogramming and cancer. Image by ClearScience

How does a single cell give rise to a fully formed organism? Insights from induced pluripotent stem (iPS) cells – cells whose developmental clocks have been wound backward to an earlier time – have helped scientists develop a deeper understanding of this process. Since scientists discovered how to create iPS cells seven years ago, researchers have begun to see parallels between the steps required to make iPS cells in the dish and the molecular events that unleash a cancer cell. In a review article published this week in Science, three researchers from the Broad Institute and Massachusetts General Hospital – Brad Bernstein, Mario Suvà, and Nicolo Riggi, describe deep insights that have been gained about features shared between oncogenesis (development of cancer) and induced pluripotency as well as directed differentiation (manipulating stem cells to become particular kinds of cells).

Many of these common features are not found within genes. Instead, events occur in the epigenome, which literally translates to “on top of” the genome. Epigenomics looks beyond our DNA sequence at the stable factors that change our genetic instructions.

Bernstein, a Broad associate member and a professor of pathology at Massachusetts General Hospital, has been studying the role of epigenomics in development and human cancer for the last 14 years. Bernstein answered several of our questions about epigenomics back in 2010. Below is an excerpt from our original interview:

Image by Maria Nemchuk, Broad Communications

Q: Can you give a couple of visible examples of epigenetics in action?

Brad Bernstein: The calico cat is a fun example. Calico cats are always female so they have two X-chromosomes. The different patches of fur color occur because there is a gene for coat color on the X, which is selectively inactivated in clonal patches of cells. The inactivation occurs by chemical modification of the DNA – there is no change in the DNA sequence – so it’s epigenetic. A less fun example is that epigenetic events also contribute to many types of cancer.

Q: Why did you decide to study epigenomics?

BB: I liked that it was uncharted territory. It was also clear early on that the tools of genomics had the potential to transform a field. So it was a good fit for me, and the Broad.

Q: What’s your favorite thing about working at the Broad Institute and Harvard-affiliated hospitals?

BB: I like working with interesting and capable people who think about big problems. There is also a lot of dedication to the mission, and people across the institution are always enthusiastic about moving science forward.

Q: What are a couple of the big questions in science that you would like to see answered in the next ten years?

BB: A big question in our field is the relationship between environment and the epigenome. We know that environmental cues can be remembered for a long-time – for example, in utero starvation can have long-term health consequences. We also know from model organism studies that certain chromatin structures are inherited when cells divide. There is some reason to think these two observations are related. But it’s really not clear at this point. My hope is that new tools for more precise and comprehensive analysis of the epigenome can begin to address this question and eventually help us understand how environment or perhaps even stochastic changes in chromatin contribute to human disease.